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Air pollution causing oxidative stress 空气污染导致氧化应激
IF 4.6
Current opinion in toxicology Pub Date : 2020-04-01 DOI: 10.1016/j.cotox.2020.02.006
Zaira Leni, Lisa Künzi, Marianne Geiser
{"title":"Air pollution causing oxidative stress","authors":"Zaira Leni,&nbsp;Lisa Künzi,&nbsp;Marianne Geiser","doi":"10.1016/j.cotox.2020.02.006","DOIUrl":"10.1016/j.cotox.2020.02.006","url":null,"abstract":"<div><p>Air pollution remains a major factor for adverse health effects and premature death worldwide. Particulate matter with aerodynamic diameter ≤2.5 μm (PM<sub>2.5</sub>), mainly originating from combustion processes, is considered most toxic. The respiratory and cardiovascular system are particularly affected. Despite all research efforts, the causative relations of air pollutants and exposure-associated health effects are not yet fully established. Recent studies using different methodologies have consistently shown peroxides and reactive oxygen species (ROS) to be crucial mediators of particle toxicity. This review is an excerpt of results from experimental studies and methodological developments of the past 2 years that enhanced our understanding of oxidative molecules in particles, their transmission to the target organ, and the molecular pathways generating ROS in physiological and pathological processes. Further multidisciplinary research towards predicting toxicology from particle-related ROS transmitted to the target organ is required.</p></div>","PeriodicalId":93968,"journal":{"name":"Current opinion in toxicology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2020-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cotox.2020.02.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46697698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 45
Cellular targets of oxidative stress 氧化应激的细胞靶点
IF 4.6
Current opinion in toxicology Pub Date : 2020-04-01 DOI: 10.1016/j.cotox.2020.05.002
Lynette K. Rogers
{"title":"Cellular targets of oxidative stress","authors":"Lynette K. Rogers","doi":"10.1016/j.cotox.2020.05.002","DOIUrl":"10.1016/j.cotox.2020.05.002","url":null,"abstract":"<div><p><span><span><span>There are three major sites of oxidant production in the cell; mitochondria, endoplasmic reticulum (ER), and </span>peroxisomes. Each is equipped with their own antioxidant system to prevent injury and protect subcellular functions. Mitochondria are essential to produce energy through </span>respiratory chain<span> activity and injury involves disruption of respiratory complexes and accelerated production and release of O2ˉ˙. ER is essential for protein processing and Ca</span></span><sup>2+</sup><span><span> homeostasis<span>, and interruption of ER functions results in upregulation of the unfolded protein response and initiation of </span></span>ER stress. Uncontrolled ER stress results in aberrant Ca</span><sup>2+</sup><span> regulation, production and release of reactive oxygen species, and activation of autophagy and apoptosis pathways. Peroxisomal function is tightly correlated to both mitochondria and ER and disruption precipitates release of H</span><sub>2</sub>O<sub>2</sub><span> into the cellular milieu. Drugs, environmental toxins, and aging all contribute to organelle injury and release of ROS, resulting in cardiovascular and neurological diseases and cancers.</span></p></div>","PeriodicalId":93968,"journal":{"name":"Current opinion in toxicology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2020-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cotox.2020.05.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49281471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Effects of combustible tobacco smoking and novel tobacco products on oxidative stress: Different sides of the same coin? 可燃烟草和新型烟草制品对氧化应激的影响:同一枚硬币的不同侧面?
IF 4.6
Current opinion in toxicology Pub Date : 2020-04-01 DOI: 10.1016/j.cotox.2020.05.001
Gavriella Kostelli, Kallirhoe Kourea, Ignatios Ikonomidis
{"title":"Effects of combustible tobacco smoking and novel tobacco products on oxidative stress: Different sides of the same coin?","authors":"Gavriella Kostelli,&nbsp;Kallirhoe Kourea,&nbsp;Ignatios Ikonomidis","doi":"10.1016/j.cotox.2020.05.001","DOIUrl":"10.1016/j.cotox.2020.05.001","url":null,"abstract":"<div><p><span>Oxidative stress<span> is the result of the imbalance between reactive oxygen species (ROS) production and antioxidant cellular systems. Smoking is one of the most important contributing factors to increased oxidative stress. Free radicals (ROS) after cigarette smoking are generated through an exogenous pathway from inhaled toxic gases in cigarette vapor or particulate phases of cigarette smoke, activation of macrophages and neutrophils </span></span><em>in situ</em><span><span>, platelet activation<span> as well as from an endogenous pathway (nitric oxide synthase, xanthine oxidase and mitochondrial electron transport chain). Furthermore, cigarette smoking weakens intracellular antioxidant mechanisms. This review focuses on the effects of conventional smoking and medically aided </span></span>smoking cessation on oxidative stress and the effects the new smoking-like devices: HNBC (heat-not-burn tobacco cigarettes) and ENDS (electronic nicotine delivery system) on oxidative burden.</span></p></div>","PeriodicalId":93968,"journal":{"name":"Current opinion in toxicology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2020-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cotox.2020.05.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45826227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 8
Gain of function mechanisms triggering biological effects of oxidized phospholipids 氧化磷脂触发生物学效应的功能机制
IF 4.6
Current opinion in toxicology Pub Date : 2020-04-01 DOI: 10.1016/j.cotox.2020.08.002
Olga V. Oskolkova, Valery N. Bochkov
{"title":"Gain of function mechanisms triggering biological effects of oxidized phospholipids","authors":"Olga V. Oskolkova,&nbsp;Valery N. Bochkov","doi":"10.1016/j.cotox.2020.08.002","DOIUrl":"10.1016/j.cotox.2020.08.002","url":null,"abstract":"<div><p><span>Oxidized phospholipids (OxPLs) are known to induce in cultured cells multiple biological effects that are potentially relevant to pathology. However, until recently it was not clear if accumulation of OxPLs plays a causative role in disease or is an epiphenomenon. Recent progress in identification of molecular targets of OxPLs led to development of new </span><em>in vivo</em><span> models that clearly demonstrated the importance of these lipid mediators in pathology. This review discusses currently known receptor and non–receptor-dependent mechanisms triggering biological action of OxPLs. Rapidly accumulating evidence suggests that some of these mechanisms represent promising targets for therapy.</span></p></div>","PeriodicalId":93968,"journal":{"name":"Current opinion in toxicology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2020-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cotox.2020.08.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44175462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
The role of oxidant stress in acetaminophen-induced liver injury 氧化应激在对乙酰氨基酚所致肝损伤中的作用
IF 4.6
Current opinion in toxicology Pub Date : 2020-04-01 DOI: 10.1016/j.cotox.2020.03.003
Hartmut Jaeschke, Anup Ramachandran
{"title":"The role of oxidant stress in acetaminophen-induced liver injury","authors":"Hartmut Jaeschke,&nbsp;Anup Ramachandran","doi":"10.1016/j.cotox.2020.03.003","DOIUrl":"10.1016/j.cotox.2020.03.003","url":null,"abstract":"<div><p>Acetaminophen<span> is a widely used analgesic and antipyretic, which can cause liver injury after an overdose. Although a controversial topic for some time, solid evidence for a critical role of oxidative and nitrosative stress has emerged during the last two decades. This review will discuss the cellular sources, amplification mechanisms, and the consequences of the excessive formation of reactive oxygen and nitrogen species in the clinically relevant mouse model of acetaminophen hepatotoxicity. This new mechanistic insight contributes to the better understanding of the mechanism of action of N-acetylcysteine, the only clinically approved antidote. In addition, it provides the rationale for the development of new antidotes that target the formation or metabolism of mitochondrial superoxide.</span></p></div>","PeriodicalId":93968,"journal":{"name":"Current opinion in toxicology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2020-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cotox.2020.03.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37852284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 11
Molecular role of cytochrome P4501A enzymes in oxidative stress 细胞色素P4501A酶在氧化应激中的分子作用
IF 4.6
Current opinion in toxicology Pub Date : 2020-04-01 DOI: 10.1016/j.cotox.2020.07.001
Rachel Stading, Chun Chu, Xanthi Couroucli, Krithika Lingappan, Bhagavatula Moorthy
{"title":"Molecular role of cytochrome P4501A enzymes in oxidative stress","authors":"Rachel Stading,&nbsp;Chun Chu,&nbsp;Xanthi Couroucli,&nbsp;Krithika Lingappan,&nbsp;Bhagavatula Moorthy","doi":"10.1016/j.cotox.2020.07.001","DOIUrl":"10.1016/j.cotox.2020.07.001","url":null,"abstract":"<div><p><span><span><span><span>Cytochrome P4501A (CYP1A) </span>enzymes play important roles in </span>xenobiotic<span> and endobiotic metabolism. Owing to uncoupling reactions during the enzymatic cycle, CYP1A enzymes can release reactive oxygen species (ROS) in the form of superoxide radical, hydrogen peroxide, </span></span>hydroxyl radical<span>, etc. An imbalance between production of free radicals and the ability of antioxidants to detoxify the free radicals can lead to accumulation of ROS, which in turn can lead to oxidative stress. Oxidative stress can lead to inflammation and toxicity, which in turn can cause human diseases such as bronchopulmonary disease, acute respiratory distress syndrome, </span></span>renal hypertension, etc. CYP1A enzymes, depending on the organ system, they either contribute or protect against oxidative injury. Thus, they have dual roles in regard to oxidative stress. This review presents an overview of the mechanistic relationship between CYP1A enzymes and oxidative stress in relation to various diseases in different organs (e.g. liver, lungs, heart, kidneys, and reproductive organs).</p></div>","PeriodicalId":93968,"journal":{"name":"Current opinion in toxicology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2020-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cotox.2020.07.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38343205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 23
Antibiotics-induced oxidative stress 抗生素引起的氧化应激
IF 4.6
Current opinion in toxicology Pub Date : 2020-04-01 DOI: 10.1016/j.cotox.2020.03.004
André Guillouzo, Christiane Guguen-Guillouzo
{"title":"Antibiotics-induced oxidative stress","authors":"André Guillouzo,&nbsp;Christiane Guguen-Guillouzo","doi":"10.1016/j.cotox.2020.03.004","DOIUrl":"10.1016/j.cotox.2020.03.004","url":null,"abstract":"<div><p><span><span>Around one hundred drugs of our modern pharmacopeia are efficacious and useable as antibiotics (ATBs) in medicine; they are used to kill or block growth of bacteria. Bactericidal ATBs can induce a common oxidative damage pathway, leading to the production of reactive oxygen species and cell death. ATBs can also damage various </span>mammalian cell<span> types and tissues but mechanisms of action remain relatively unclear. Both bactericidal and bacteriostatic ATBs can target mitochondria but only the former usually induce mitochondrial dysfunction and oxidative stress<span> at clinically relevant doses. Human liver is a major target of ATBs of which toxicity is mostly idiosyncratic. Interestingly, β-lactam penicillinase-resistant ATBs, which are known to cause mostly immune reactions in patients, induce an early endoplasmic reticulum stress in </span></span></span><em>in vitro</em><span> human hepatocytes at low concentrations; this stress is inhibited by activation of the HSP27 protein which acts as a protective response associated with occurrence of cholestatic features. In this review, we analyze the importance of oxidative and endoplasmic reticulum stress in cellular damage induced by ATBs, especially in hepatocytes and highlight specific cellular protection mechanisms associated with penicillinase-resistant ATB treatments.</span></p></div>","PeriodicalId":93968,"journal":{"name":"Current opinion in toxicology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2020-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cotox.2020.03.004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44624555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 7
Editorial review: Molecular role of reactive oxygen species in oxidative stress: Mechanisms, cellular targets, and human diseases 编辑综述:活性氧在氧化应激中的分子作用:机制、细胞靶点和人类疾病
IF 4.6
Current opinion in toxicology Pub Date : 2020-04-01 DOI: 10.1016/j.cotox.2020.10.001
Rachel Stading, Bhagavatula Moorthy
{"title":"Editorial review: Molecular role of reactive oxygen species in oxidative stress: Mechanisms, cellular targets, and human diseases","authors":"Rachel Stading,&nbsp;Bhagavatula Moorthy","doi":"10.1016/j.cotox.2020.10.001","DOIUrl":"10.1016/j.cotox.2020.10.001","url":null,"abstract":"","PeriodicalId":93968,"journal":{"name":"Current opinion in toxicology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2020-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cotox.2020.10.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43914100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Plastics and plastic additives as inducers of oxidative stress 作为氧化应激诱导剂的塑料和塑料添加剂
IF 4.6
Current opinion in toxicology Pub Date : 2020-04-01 DOI: 10.1016/j.cotox.2020.07.002
Elisabet Pérez-Albaladejo , Montserrat Solé , Cinta Porte
{"title":"Plastics and plastic additives as inducers of oxidative stress","authors":"Elisabet Pérez-Albaladejo ,&nbsp;Montserrat Solé ,&nbsp;Cinta Porte","doi":"10.1016/j.cotox.2020.07.002","DOIUrl":"10.1016/j.cotox.2020.07.002","url":null,"abstract":"<div><p><span><span>As plastics in the environment break down to smaller particles, contain additives, trap environmental pollutants and cross cell membranes, there is growing concern about the toxicological consequences for humans and vulnerable aquatic species. Recent studies have shown the ability of plastic additives to disrupt </span>oxidative metabolism<span> and cause damage to macromolecules as part of their mechanism of action. This article focuses on human and fish cell models because they serve to unravel the mechanisms of action of plastic additives and to predict the consequences of exposure. In addition, some </span></span><em>in vivo</em><span> studies revealing the action of plastics and its additives on oxidative stress parameters in aquatic organisms are reviewed. The selected works highlight an alteration of the oxidative stress balance as one accepted mechanism of action of plastics and warn about the negative consequences on humans and wildlife.</span></p></div>","PeriodicalId":93968,"journal":{"name":"Current opinion in toxicology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2020-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cotox.2020.07.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45381424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 15
Metal-induced oxidative stress: an evidence-based update of advantages and disadvantages 金属诱导的氧化应激:基于证据的优点和缺点的更新
IF 4.6
Current opinion in toxicology Pub Date : 2020-04-01 DOI: 10.1016/j.cotox.2020.05.006
Madiha Khalid, Shokoufeh Hassani, Mohammad Abdollahi
{"title":"Metal-induced oxidative stress: an evidence-based update of advantages and disadvantages","authors":"Madiha Khalid,&nbsp;Shokoufeh Hassani,&nbsp;Mohammad Abdollahi","doi":"10.1016/j.cotox.2020.05.006","DOIUrl":"10.1016/j.cotox.2020.05.006","url":null,"abstract":"<div><p>Metals are well distributed in our ecosystem and have several advantages and disadvantages. Some are well known for inducing oxidative stress<span> by disturbing the cellular redox system<span><span> and generating intracellular reactive oxygen species and are thus responsible for many pathologies. Several studies have reported metal-induced oxidative stress and the resultant poor health outcomes. However, recently, researchers have modified the oxidative stress–inducing property of metals for treatment and diagnostic purposes. They have developed various metal-based </span>nanoparticles<span>, composites, drug delivery systems, sensors, and detectors. Such products have demonstrated therapeutic potential against various cancer cell lines and microbial infections; thus, they have diagnostic potential for the detection of various oxidative stress parameters in different biological fluids.</span></span></span></p></div>","PeriodicalId":93968,"journal":{"name":"Current opinion in toxicology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2020-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cotox.2020.05.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48466288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 10
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